A number of enzymatic processes have been identified in recent years which act to repair lesions in DNA induced by alkylating agents. These enzymes include the glycosylases, Apurinic/Apyrimidinic endonucleases and the methyltransferases. The biological consequences of defects in these enzyme systems are for the most part unknown. Few mutants have been identified which are defective in these processes. The initial selection method has been to isolate mutants which are incapable of supporting growth of bacteriophage damaged by alkylating agents. Such mutants are now being screened for sensitivity to alkylating agents. By this method, we expect to accumulating strains containing mutations in the enzymes responsible for repair of alkylated DNA as well as mutations in genes which regulate these enzymes or permit their expression. Such mutants will permit the systematic evaluation of the relative roles these repair enzymes perform in the recovery from alkylation damage, evaluation of the mutagenic properties of the lesions upon which specific enzymes act and identification of the genes which code for these enzymes.